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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Escherichia coli O78: K80 strains isolated from an outbreak among premature and newborn infants with meningitis, sepsis and enteritis, from sporadic cases of enteritis and from healthy carriers were compared with one another and with different E. coli serogroups. The O78: K80 cultures uniformly failed to give the rabbit intestinal loop test and the guinea pig eye reaction and none of them contained L1 antigen. After intraperitoneal injection into mice, the organisms multiplied in the peritoneal cavity and caused bacteriaemia lasting at least 2 weeks. E. coli strains originating from septicaemia (O78: K80, O18a,c: K?, O83: K?) showed significantly lower LD50 values for mice (9 x 10(3)--7 x 10(5)) than did E. coli serogroups associated with infantile enteritis only (3 x 10(8)--7 x 10(8)). It is assumed that the isolates differ in pathogenicity not only from E. coli strains associated with "cholera-like" disease and with "dysenteriform" infection, but also from L1 antigen-containing cultures described in neonatal meningitis, and constitute a separate group characterized by an ability to cause meningitis, sepsis and enteritis within the same outbreak.
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PMID:Characterization of Escherichia coli serogroups causing meningitis, sepsis and enteritis. I. Serological properties and animal pathogenicity of O18, O78 and O83 isolates. 34 52

Escherichia coli O78: K80 strains isolated from an outbreak of meningitis, sepsis and enteritis in infants, were compared with O78: K80 strains from sporadic cases of enteritis, healthy carriers and animals. The strains were uniform in antigenic structure and phage pattern but differed in colicinogenicity. The epidemic strains and calf-pathogenic cultures produced colicin V, the remaining isolates were characterized by other types of colicin or were not colicinogenic. Col V+ strains multiplied in the mouse peritoneal cavity more readily and killed the animals at significantly lower doses than did col V- strains. One half of antibiotic resistant O78: K80 strains carried R factor. The spread of R factor could be followed by phage restriction experiments.
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PMID:Characterization of Escherichia coli serogroups causing meningitis, sepsis and enteritis. II. Classification of Escherichia coli O78 strains by phage sensitivity, colicin type and antibiotic resistance. 34 53

Fimbriae were purified from Escherichia coli strains isolated from chickens with septicemia or colibacillosis. When grown on solid media, these strains expressed fimbriae with an apparent subunit molecular mass of 18 kDa. Morphological, biochemical, serological, functional, and molecular characterization revealed that these 18-kDa fimbriae are identical to F11 fimbriae, which were previously found to be involved in the pathogenesis of human urinary tract infection. Screening of a large strain collection showed that 78% of chicken E. coli strains expressed F11 fimbriae, whereas this percentage increased to 96% when the only strains taken into account were those with the serotypes most commonly encountered in avian colibacillosis (O1:K1, O2:K1, O35, and O78:K80). The prevalence of F11 fimbrial expression appeared to be independent of the country of isolation of the strains, except for the United States, where the prevalence seemed higher. Expression of F11 fimbriae by chicken E. coli strains could not be correlated with adherence to chicken tracheal or pharyngeal cells.
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PMID:Identification of F11 fimbriae on chicken Escherichia coli strains. 809 82

The avian pathogenic Escherichia coli strain (chi)7122 (serotype O78:K80:H9) causes airsacculitis and colisepticemia in chickens. To identify genes associated with avian disease, a genomic subtraction technique was performed between strain (chi)7122 and the E. coli K-12 strain (chi)289. The DNA isolated using this method was found only in strain (chi)7122 and was used to identify cosmid clones carrying unique DNA from a library of (chi)7122 that were then used to map the position of unique DNA on the E. coli chromosome. A total of 12 unique regions were found, 5 of which correspond to previously identified positions for unique DNA sequence in E. coli strains. To assess the role each unique region plays in virulence, mutants of (chi)7122 were constructed in which a segment of unique DNA was replaced with E. coli K-12 DNA by cotransduction of linked transposon insertions in DNA flanking the unique sequence. The resulting replacement mutants were assessed for inability to colonize the air sac and cause septicemia in 2-week-old white Leghorn chickens. Two mutants were found to be avirulent when injected into the right caudal air sac of 2-week-old chickens. One avirulent mutant, designated (chi)7145, carries a replacement of the rfb locus at 44 min, generating a rough phenotype. The second mutant is designated (chi)7146, and carries a replacement at position 0.0 min on the genetic map. Both mutants could be complemented to partial virulence by cosmids carrying sequences unique to (chi)7122.
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PMID:Unique chromosomal regions associated with virulence of an avian pathogenic Escherichia coli strain. 885 24

Infections with avian pathogenic Escherichia coli (APEC) cause colibacillosis, an acute and mostly systemic disease resulting in significant economic losses in poultry industry worldwide. Avian colibacillosis is a complex syndrome characterized by multiple organ lesions with airsacculitis and associated pericarditis, perihepatitis and peritonitis being most typical. Environmental factors as well as the constitution of poultry or initial viral infections influence the outcome of APEC-infections. However, several challenge experiments in chickens proofed the role of virulent APEC strains as the single aetiological agent. Currently serotypes O1:K1, O2:K1 and O78:K80 are recognized as the most prevalent, however the number of published serotypes is increasing. In addition, single APEC isolates vary profoundly in virulence, and knowledge about the molecular basis of this variability is still scarce. Known virulence factors of APEC are adhesins (F1- and P-fimbriae), iron acquisition systems (aerobactin and yersiniabactin), hemolysins (hemolysinE and temperaturesensitive hemagglutinin), resistance to the bactericidal effects of serum and phagocytosis (outer membrane protein, iss protein, lipopolysaccharide, K/1)-capsule and colilcin production) as well as toxins and cytotoxins (heat stable toxin, cyto-/verotoxin and flagella toxin). Esperimental studies have shown that the respiratory tract, principally the gas-exchange region of the lung and the interstitium of the air sacs are the most important sites of entry for avian pathogenic E. coli. APEC strains adhere to the epithelial cells of air sacs presumably through F1-fimbriae. After colonization and multiplication the bacteria enter the bloodstream, and the temperature-sensitive hemagglutinin (tsh) seems to be important int his step. After invading the bloodstream APEC cause a septicemia resulting in massive lesins in multiple internal organs and in sudden death of the birds. The ability of the bacteria to acquire iron and the resistance to the bactericidal effects of serum, predominantly conferred by the increased serum survival (iss)--protein, enables APEC to multiply quickly in their hosts. Iss is regarded a specific genetic marker for avian pathogenic E. colistrains. A critical review of the literature published so far on APEC reveals, that these pathotypes are not defined appropriately. This findings urge investigations on the population structure of APEC, enabling the establishment of appropriate diagnostic tools and avoiding the obsolete use of serotyping for APEC diagnosis. So far more than 20 APEC strains have been investigated in animal experiments, explaining contrary published results. Thus, the lack of knowledge in pathogenicity and in immunity of APEC infections urges further experimental studies. As APEC share not only identical serotypes with human pathogens but also specific virulence factors, their zoonotic potential is under consideration.
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PMID:[Avian pathogenic Escherichia coli (APEC)]. 1452 68

Escherichia coli O78 strains are frequently associated with extraintestinal diseases, such as airsacculitis and septicemia, in poultry, livestock, and humans. To understand the influence of the pst operon in the virulence of E. coli, we introduced mutations into the pst genes of the avian pathogenic E. coli (APEC) O78:K80 strain chi7122 by allelic exchange. The mutation of pst genes led to the constitutive expression of the Pho regulon. Furthermore, the virulence of APEC strain chi7122 in a chicken infection model was attenuated by inactivation of the Pst system. The pst mutant caused significantly fewer extraintestinal lesions in infected chickens, and bacterial numbers isolated from different tissues after infection were significantly lower for the mutant than for the wild-type strain. Moreover, resistance to the bactericidal effects of rabbit serum and acid shock was impaired in the pst mutant, in contrast to the wild-type strain. In addition, the MIC of polymyxin was twofold lower for the mutant than for the wild-type strain. Although the pst mutant demonstrated an increased susceptibility to rabbit serum, this strain was not killed by chicken serum, suggesting the presence of differences in host innate immune defenses and complement-mediated killing. In APEC O78 strain chi7122, a functional Pst system is required for full virulence and resistance to acid shock and polymyxin. Our results suggest that the mutation of pst genes induces a deregulation of phosphate sensing and changes in the cell surface composition that lead to decreased virulence, indicating the importance of the Pst system for the virulence of pathogenic E. coli strains from different hosts.
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PMID:Inactivation of the pst system reduces the virulence of an avian pathogenic Escherichia coli O78 strain. 1597 3